pistonpump
Banned
tamoxifen is better. end of story cuz i said so. 
tamoxifen is better. end of story cuz i said so.![]()
anpother good posting!!!
ive been trying to show people all things prolactin related, happen when something interacts with the 5a Reductase. (i havent seen many people using clomid, only nolva) nolva can sensitize certain receptors and BAM prolactin and gyno after post cycle.
CLOMID is always better, it mimics the pituitary instead of just blocking estrogen in the hypothalmus, causing a much better signal to the testes.
clomid is especially better when running something that interacts with the 5a reductase.
I say SOMEHOW 2 of us get bloods done before our cycle, then again 2 weeks into PCT. 1 uses tamox, the other clomid. Post the results, see who does the best job at restoring HPTA function.Clomid FTW!! :head:
i have some stuff at home on this whole issue, im in DC till late tonight, should be home to shed some more researched based light on this.
especially with the tamoxifen and decreased IGF1 and clomid vs nolva,
it seems as though becuase nolva stimulates the hypothalamus by means of an anti estrogen it indirectly icreases test LH ect, where as clomid mimics the pituitary hormone which directly stimulates the release.
I with you on this pct for normal test and most designers. I still feel strongly that an AI is not necessarily a good idea on superdrol...........Slippery slope. 6-oxo maybe, definately no ldex.
Heres a lot of "real world" ancedotes of men using clomid and or HCG to bring test back. Interesting read.
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Why are more doctors using clomid to recover test and sperm count than nolva if they "do the same thing"?
Another excerpt plagerized from the net.
Concerning the length of a clomid protocol.
"The claim that duration of intake should not exceed 10-14 days is incorrect. Clinical studies with male patients have been for periods of a year or longer. This error probably originates from the fact that, for use in women, due to the menstrual cycle there would obviously be no point in trying to stimulate ovulation all four weeks of the month. Thus, use in women is limited to 10-14 days. That limitation is not because of toxicity."
I have searched and searched, there is just very little actual reliable real world data on either nolva or clomid in the male........THat i can find....... Most of it is all based on females.
I still prefer clomid over Nolva for actual test recovery. Nolva for E blocker, in typical test cycles............. Not counting gynodrol.
Clomid, Nolvadex, and Testosterone Stimulation
By: William Llewellyn
Introduction
I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell.
And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.
Clomid and Nolvadex
I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor.
In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.
Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant.
What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration. We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.
Pituitary Sensitivity to GnRH
But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response.
The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment).
As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.
The Estrogen Clomid
The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".
Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2).
This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.
Conclusion
To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid.
This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.
Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well.
Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.
In next month's follow-up article I will be discussing the role anti-estrogens play in post-cycle testosterone recovery. Most specifically, I will be detailing what a proper post-cycle ancillary drug program looks like, and explain why anti-estrogens alone are not effective during this window of time.
I will volunteer to do the clomid protocol.........I could get away with post cycle and post pct........ Thats about the best i could do....... I explained my reasoning in a previous post in this thread.
i have some stuff at home on this whole issue, im in DC till late tonight, should be home to shed some more researched based light on this.
especially with the tamoxifen and decreased IGF1 and clomid vs nolva,
it seems as though becuase nolva stimulates the hypothalamus by means of an anti estrogen it indirectly icreases test LH ect, where as clomid mimics the pituitary hormone which directly stimulates the release.
Document title
Clomiphene citrate reduces serum insulin-like growth factor I and increases sex hormone-binding globulin levels
Author(s)
BÜTZOW T. L. ; KETTEL L. M. ; YEN S. S. C. ;
Author(s) Affiliation(s)
Univ. California, school medicine, dep. reproductive medicine, San Diego La Jolla CA 92093-0802, ETATS-UNIS
Résumé / Abstract
Objectives: To evaluate the effect of clomiphene citrate (CC) on circulating levels of insulin-like growth factor I (IGF-I) and sex hormone-binding globulin (SHBG) in patients with polycystic ovary syndrome (PCOS). Design: Prospective open trial. Patients: Eight women with clinical and biochemical evidence of PCOS. Intervention: One hundred fifty milligrams CC was administered orally for 5 days. Main Outcome Measures: Serum IGF-I, SHBG, LH, FSH, and E2 levels were determined for 8 days, beginning 3 days before CC treatment. Results: A progressive decline in serum IGF-1 levels was observed in all subjects reaching a maximum of 30% on the 5th day of therapy (40.6±5.1 to 28.7±4.0 nmol/L [conversion factor to SI unit, 0.13]). This was correlated inversely with the expected rises in LH, FSH, and E2 levels. Concomitantly, there was a 23% rise in SHBG levels. The absolute decrease of IGF-I levels was negatively correlated with age and was independent of body mass index. Conclusions: These observations suggest that oral administration of CC has an impact on the IGF-I and SHBG systems, which may be involved in the initiation of ovulatory function in PCOS
Clomiphene citrate increases insulin-like growth factor binding protein-1 and reduces insulin-like growth factor-I without correcting insulin resistance associated with polycystic ovarian syndrome.
V de Leo, A la Marca, G Morgante, L Ciotta, L Mencaglia, A Cianci, F Petraglia
Department Obstetrics and Gynecology, University of Study of Siena, Italy. [email protected]
The induction of ovulation by clomiphene could be the result of interaction of the drug at various levels: hypothalamus, pituitary and ovary. It was demonstrated that administration of clomiphene to women with polycystic ovarian syndrome (PCOS) is accompanied by a reduction in plasma concentrations of insulin-like growth factor-I (IGF-I). IGF-I seems to have an overall negative effect on normal folliculogenesis and ovulation. The aim of the present study was to evaluate the effect of clomiphene on plasma concentrations of IGF-I and IGF binding protein (IGFBP)-1 and on insulin resistance associated with PCOS. Fifteen patients diagnosed with PCOS were recruited. Clinical diagnosis was based on chronic oligomenorrhoea or amenorrhoea and hyperandrogenaemia. Clomiphene citrate was administered at a dose of 100mg/day to all women from day 5 to day 9 of the spontaneous or medroxyprogesterone acetate (MAP)-induced menstrual cycle. Blood sampling and a 2 h oral glucose loading test (75 g) were performed the day before and after the course of clomiphene. Ovulation was confirmed in 13/15 PCOS patients. Plasma concentrations of IGF-I decreased by 31.5% (434 +/- 84 versus 297 +/- 71 ng/ml; P: < 0.05) after 5 days of clomiphene therapy, whereas plasma concentrations of IGFBP-1 increased by approximately 28.1% (26.3 +/- 4 versus 36.6 +/- 7 ng/ml; P: < 0.05). This gave a 56.5% reduction in the IGF-I:IGFBP-1 ratio (21.9 versus 9.53). No significant changes in basal plasma concentrations of fasting insulin or area under the insulin curve were observed in response to oral loading. The present results show that clomiphene does not cause changes in insulin resistance associated with PCOS but reduces plasma concentrations of IGF-I and increases those of IGFBP-1, with a consequent marked reduction in the IGF-I:IGFBP-1 ratio.
And another showing IGF-1 decreasing 31.5%
Z (and others!), you've really outdone yourself in this thread. Some great info. Some I've seen before, some is new, and its all together! I am definitely voting sticky or transferring much of this to a new thread and stickying that. Maybe a clomid vs nolva sticky where everyone can post there evidence (science only, no my balls got bigger, it must work!). Mods????
And we have another on our side. Primordial Perf votes Nolva over Clomid as well:
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Evista(ralox) is actually much more common than tamox or clomid(in my pharmacy at least). Just saying...Also, adex is more popular than tamox.
How many times have you used Clomid and Nolva, being that you prefer Clomid much more?
Never nolva.........
clomid and ldex..........test cycle........no bloodwork.
clomid, ldex 1-test and 4ad......no bloodwork.
Your not gonna change my opinion on nolva, whatever stats you pull out........
Never.
Right or wrong.
Then what is your overall agenda in this conversation exactly?
to stop the propaganda machine that is building nolva up to be the end all pct..........
end gyno cases from superdrol
I am tired of seeing the gyno cases from the nolva, nolva+ ai pct protocols being shoved down superdrol users throat.
Nolva is not the end all be all pct........Its an ANTI-E...... that doesnt seem to be working for alot of superdrol users.
Whats yours?
Never nolva.........
clomid and ldex..........test cycle........no bloodwork.
clomid, ldex 1-test and 4ad......no bloodwork.
Your not gonna change my opinion on nolva, whatever stats you pull out........
Never.
Right or wrong.
Did I mention NO GYNO.
PS. I hate nolva for gynodrol.
to stop the propaganda machine that is building nolva up to be the end all pct..........
end gyno cases from superdrol
I am tired of seeing the gyno cases from the nolva, nolva+ ai pct protocols being shoved down superdrol users throat.
Nolva is not the end all be all pct........Its an ANTI-E...... that doesnt seem to be working for alot of superdrol users.
Whats yours?
Sorry to say but you sound incredibly ignorant, stubborn and dense. Never going to change you mind right or wrong, because you guess clomid worked for you and have never tried nolva?? C'mon thats not a very good end to a good discussion is it?
I don't care to be involved in this converstaion because it's a pure extension of past arguements LONG ago.
Exactly. This argument never dies.
Now everybody play nice and lets get UNC huge.![]()
Exactly. This argument never dies.
Now everybody play nice and lets get UNC huge.![]()
a female study on nolva and the PGr's
"Tamoxifen citrate increases expression of progesterone receptor.
--------------------------------------------------------------------------------
J Steroid Biochem Mol Biol. 2005 May;95(1-5):83-9.
Aromatase inhibitors: cellular and molecular effects.
Miller WR, Anderson TJ, White S, Larionov A, Murray J, Evans D, Krause A, Dixon JM.
Breast Unit, Western General Hospital, Edinburgh, Scotland, UK. [email protected]
Marked cellular and molecular changes may occur in breast cancers following treatment of postmenopausal breast cancer patients with aromatase inhibitors. Neoadjuvant protocols, in which treatment is given with the primary tumour still within the breast, are particularly illuminating. In Edinburgh, we have shown that 3 months treatment with either anastrozole, exemestane or letrozole produces pathological responses in the majority of oestrogen receptor (ER)-rich tumours (39/59) as manifested by reduced cellularity/increased fibrosis. Changes in histological grading may also take place, most notably a reduction in mitotic figures. This probably reflects an influence on proliferation as most tumours (82%) show a marked decrease in the proliferation marker, Ki67. These effects are generally more dramatic than seen with tamoxifen given in the same setting. Differences between aromatase inhibitors and tamoxifen are also apparent in changes in steroid hormone expression. Thus, immuno-staining for progesterone receptor (PgR) is reduced in almost all cases by aromatase inhibitors, becoming undetectable in many. This contrasts with effects of tamoxifen in which the most common change on PgR is to increase expression. Changes in proliferation occur rapidly following the onset of exposure to aromatase inhibitors. Thus, neoadjuvant studies with letrozole in which tumour was sampled before and after 14 days and 3 months treatment show that decreased expression of Ki67 occur at 14 days and, in many cases, the effect is greater at 14 days than 3 months. These early changes precede evidence of clinical response but do not predict for it. However, this study design has allowed RNA analysis of sequential biopsies taken during the neoadjuvant therapy. Based on clustering techniques, it has been possible to subdivide tumours into groups showing distinct patterns of molecular changes. These changes in tumour gene expression may allow definition of tumour cohorts with differing sensitivity to aromatase inhibitors and permit early recognition of response and resistance."
It's like beating a dead horse........been there, done that. It's now time to move forward.
I agree, get hyooooggeeeee UNC!!!
:bb3:
Nobody ever said Nolva was the end all PCT. Torem is just as good if not better though it's much more expensive. However Nolva is a newer, improved version of Clomid which both do the same thing, but Nolva just does it a little better/more safely (which was the conversation here). There's many PCT's one could use successfully, though SERMs seem to have people bouncing back quicker and without the cholesterol threats of AI's. But again that's not the conversation here anyhow.
As for Superdrol PCT if you're talking about gyno, these are usually people who are prone anyhow. Besides I know more who got gyno with SD from ATD than anything. Also know a guy who got gyno running Clomid and 6-OXO. But if you could post all of these enlightening links where 'alot of superdrol users' got gyno from using Nolva alone (apparently the sole cause) - that would greatly help, thanks.
Sorry to say but you sound incredibly ignorant, stubborn and dense. Never going to change you mind right or wrong, because you guess clomid worked for you and have never tried nolva?? C'mon thats not a very good end to a good discussion is it?
Sure it is. Trauma made a good point.
ALL the e-stats, pubmeds, clinicals, write ups in the world me nothing.
I am stubborn, I definately am ignorant in alot of things, I dont not claim know everything.
I have my stance on pct protocols, from what i believe to be valid data.
Have you done a taste test comparison?
No, I have never tried clomid. But I'm open minded. I have used nolva, with post PCT bloodwork (2 weeks post PCT) where I was perfectly recovered. So for me nolva works.
I am also somewhat stubborn, but we all come to these boards to learn, if your opinion wont be changed "right or wrong" why are you here? If you said 'personally I will stick with Clomid, but great info' then fair enough, but you didnt, you just made yourself look stupid.
Anyway not going to continue further hijacking UNC's thread![]()
Sure it is. Trauma made a good point.
ALL the e-stats, pubmeds, clinicals, write ups in the world me nothing.
I am stubborn, I definately am ignorant in alot of things, I do not claim know everything.
I have my stance on pct protocols, from what i believe to be valid data.
Have you done a taste test comparison?
SERM's in general aren't recommended with progestins. Superdrol isn't a progestin, I'm not sure where people get that.
Are you being sarcastic now?
Ignorance breeds nothing of any significance to any converstaion.......that is a fact.
Nobody claims to know everything here at all, but claiming superdrol pct "propoganda" while you yourself are proclaimed stubborn/ingnorant proves what exactly?
Let it die man.......
Sure it is. Trauma made a good point.
ALL the e-stats, pubmeds, clinicals, write ups in the world me nothing.
I am stubborn, I definately am ignorant in alot of things, I do not claim know everything.
I have my stance on pct protocols, from what i believe to be valid data.
Have you done a taste test comparison?
My opinion is based off a combination of clinical data, personal experience, and classes in behavioral science and medicine.
Out of curisousity, if the clinical studies showing data mean nothing to you - what's the 'valid data' that you go by then?
They are assuming that, because users have been known to lactate both on cycle and during PCT. Yes, things other than high prolactin levels can cause lactation and that will not be discussed in this thread, but i'm just saying where people "get that." TEST FTW!!!! Nobody should be taking SD anyway. Use something else and you won't even need to worry about the notorious "delayed gyno."This did not even exist prior to all of these clones that have came out, so that should tell you something.
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Whats up guys, need some good honest feedback on this cycle.
CEL PPlex and CEL Mdrol.
My Phera is the 19.2mg. So I will be rounding up.
Week 1- PP-20mg
Week 2- PP-40mg
Week 3- PP-40mg/ SD-10mg
Week 4- SD- 20mg
Week 5- SD- 20mg
Supports-
Pre-Load Cycle Support
Liver Longer/Cycle Support
Taruine
ACES/NoXidant
Gut Health-
PCT-
Nolva- 40,20,20,10mg
Clomid-????
6-OXO- 600,600,300,300mg or Inhibit-E 3,2,2,1
Taurine
ACES/NoXidant
Gut Health
SAMe- 600,600,400,400mg
Cycle Support
SizeON
Purple Wraath
Intracell
Thoughts on Clomid doses? Also thoughts on Phera doses and length.
Stats-
6'4
249lbs
BF- 17-18%
Exp-
3AD
Epi-E
Halodrol-50/Orastan-E
Hemadrol/Propadrol
Edit- I forgot to mention the on and off cycle addition of ALCAR.
I'll third that
Though you sig does seem somewhat relevant to this thread :toofunny:
SERM's in general aren't recommended with progestins. Superdrol isn't a progestin, I'm not sure where people get that.
SERM's in general aren't recommended with progestins. Superdrol isn't a progestin, I'm not sure where people get that.
they think bc of the prolactin sides, relate prolactin to tren deca ect and then get the same leaky nips from superdrol
Hmmm... then it seems babies are progestins too![]()
Indeed they are![]()